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A Tissue-Specific Scaffold for Tissue Engineering-Based Ureteral Reconstruction
Terminally differentiated somatic cells can rapidly change phenotypes when they are isolated from their native tissue and cultured in vitro. This problem may become a barrier to tissue engineering-based organ reconstruction, which utilizes somatic cells. The present study was designed to validate th...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4361581/ https://www.ncbi.nlm.nih.gov/pubmed/25775033 http://dx.doi.org/10.1371/journal.pone.0120244 |
Sumario: | Terminally differentiated somatic cells can rapidly change phenotypes when they are isolated from their native tissue and cultured in vitro. This problem may become a barrier to tissue engineering-based organ reconstruction, which utilizes somatic cells. The present study was designed to validate the feasibility of maintaining the urothelial cell phenotype in a tissue-specific ureteral scaffold. The tissue-specific scaffold was fabricated by blending poly (L-lactic acid) (PLLA) and ureteral extracellular matrix (UECM) using electrostatic spinning technology. PLLA was used to enhance the mechanical properties, and UECM was used to mimic the natural components of the ureter. Primary urothelial cells (UCs), derived from ureteral mucosa, were seeded onto the tissue-specific scaffold to assess cell adhesion, proliferation and phenotypes at designated time points. The results showed that UCs in the tissue-specific scaffold exhibited better proliferation compared to cells in pure PLLA or a PLLA-small intestinal submucosa (PLLA-SIS) scaffold (p<0.05). At different time points, the expression of a UC-specific marker (UroplakinⅢ) in the tissue-specific scaffold was significantly higher than its expression in pure PLLA or a PLLA-SIS scaffold (p<0.05). Therefore, the tissue-specific scaffold appears to be an ideal substrate for promoting UC survival and phenotype maintenance. |
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